College of Life Science, Shandong Normal University, Jinan, Shandong, 250014, China.
Plant J. 2010 May 1;62(4):539-48. doi: 10.1111/j.1365-313X.2010.04173.x.
AtFes1A is induced by high temperatures, and encodes a protein containing the armadillo repeat motif. Little is known about its biological function, however. In this study, we observed an increased heat-sensitive phenotype in atfes1a mutants, suggesting the involvement of AtFes1A in acquired thermotolerance. We found that AtFes1A is cytosolic and associates with cytosolic Hsp70. Loss of AtFes1A leads to a selective reduction of cytosolic Hsp70 and a global increase in heat shock transcription. Thus, AtFes1A appears to prevent cytosolic Hsp70 degradation, and acts as a negative regulator of heat-shock transcription. We also found increased ubiquitination of total protein in atfes1a mutants after severe heat stress. These findings suggest that AtFes1A plays an important role in heat response signalling pathways, in addition to its role in thermotolerance.
AtFes1A 受高温诱导，编码一种含有类角蛋白重复模体的蛋白质。然而，关于其生物学功能知之甚少。在这项研究中，我们观察到 atfes1a 突变体表现出对高温敏感的表型增加，表明 AtFes1A 参与了获得性耐热性。我们发现 AtFes1A 是细胞质的，并与细胞质 Hsp70 相关联。AtFes1A 的缺失导致细胞质 Hsp70 的选择性减少和热休克转录的全局增加。因此，AtFes1A 似乎可以防止细胞质 Hsp70 的降解，并作为热休克转录的负调节剂。我们还发现严重热应激后 atfes1a 突变体中的总蛋白泛素化增加。这些发现表明，AtFes1A 除了在耐热性中发挥作用外，还在热应激信号通路中发挥重要作用。
